Harrisnoel2316

Background Studies have shown inconsistent results regarding the diagnostic performance of ultrasound elastography for axillary lymph node metastasis (ALNM) in breast cancer. This meta-analysis aimed to estimate the diagnostic performance of ultrasound elastography (divided into quantitative and qualitative elastography) for ALNM in patients with breast cancer. Methods The PubMed and Embase databases were searched for eligible studies exploring the diagnostic performance of ultrasound elastography for ALNM in patients with breast cancer. The included studies were divided into quantitative and qualitative elastography groups to perform separate meta-analyses. The diagnostic performance was investigated with pooled sensitivity and specificity and diagnostic odds ratio (DOR) using a bivariate mixed-effects regression model. A summary receiver operating characteristic curve was constructed, and the area under the curve (AUC) was calculated. Results Seven and 11 studies were included in the quantitative and qualitative elastography meta-analyses, respectively. The pooled sensitivity and specificity, DOR, and AUC with their corresponding 95% confidence intervals were 0.82 (0.75, 0.87), 0.88 (0.78, 0.93), 33 (13, 83), and 0.89 (0.86, 0.91), respectively, for quantitative elastography and 0.81 (0.69, 0.89), 0.92 (0.79, 0.97), 46 (12, 181), and 0.92 (0.89, 0.94), respectively, for qualitative elastography. No significant publication bias existed. Fagan plots demonstrated good clinical utility. However, substantial heterogeneity existed among studies. Study design, measurement, and reference standard served as potential sources of heterogeneity for quantitative studies, which were measurement and reference standard for qualitative studies. Conclusions Both quantitative and qualitative elastography seem to be feasible, non-invasive diagnostic tools for ALNM in breast cancer. Nevertheless, the results must be interpreted carefully, paying attention to heterogeneity issues, especially for quantitative elastography studies.Partial hepatectomy (PH) is the main treatment for early-stage hepatocellular carcinoma (HCC). Selleck HIF inhibitor Yet, a significant number of patients undergo recursion of the disease that could be linked to the fate of innate immune cells during the liver regeneration process. In this study, using a murine model, we investigated the impact of PH on HCC development by bioluminescence imaging and flow cytometry. While non-resected mice were able to control and reject orthotopic implanted Hepa1-6 hepatocarcinoma cells, resected liver underwent an increased tumoral proliferation. This phenomenon was associated with a PH-induced reduction in the number of liver-resident macrophages, i.e., Kupffer cells (KC). Using a conditional ablation model, KC were proved to participate in Hepa1-6 rejection. We demonstrated that in the absence of Hepa1-6, PH-induced KC number reduction was dependent on tumor necrosis factor-alpha (TNF-α), receptor-interacting protein kinase (RIPK) 3, and caspase-8 activation, whereas interleukin (IL)-6 acted as a KC pro-survival signal. In mice with previous Hepa1-6 encounter, the KC reduction switched toward a TNF-α-RIPK3-caspase-1 activation. Moreover, KC disappearance associated with caspase-1 activity induced the recruitment of monocyte-derived cells that are beneficial for tumor growth, while caspase-8-dependent reduction did not. In conclusion, our study highlights the importance of the TNF-α-dependent death pathway induced in liver macrophages following partial hepatectomy in regulating the antitumoral immune responses.

Inconsistent findings from observational studies have reported that C-reactive protein (CRP) is likely associated with risk of prostate cancer. Because conventional observational studies are susceptible to confounding and reverse causality, it remains unclear whether there is a causal relationship of CRP with risk of prostate cancer.

In this study, we applied a two-sample Mendelian randomization (MR) approach to evaluate the potential causal association of circulating CRP levels with prostate cancer risk. Instrumental variables (IVs) and corresponding genetic association estimates for circulating CRP levels were obtained from a meta-analysis of genome-wide association studies (GWASs) including 204,402 participants of European descent. The genetic association estimates of these IVs with prostate cancer were obtained from a GWAS meta-analysis including 79,148 cases and 61,106 controls of European ancestry. The inverse-variance weighted (IVW) method was used as primary MR analyses, whereas in sensitivity anarisk, suggesting that CRP is unlikely to be a causal factor in the development of prostate cancer.

To analyze the role of frequency of heterotypic neutrophil-in-tumor structure (FNiT) in the prognosis of patients with buccal mucosa squamous cell carcinoma (BMSCC).

, we cocultured BMSCC cell line-H157 with neutrophils to form heterotypic neutrophil-in-tumor structures, which were then subject to fluorescence staining. Clinically, 145 patients were retrospectively enrolled. Associations between FNiT and clinicopathological variables including age, sex, smoking history, drinking history, betel nut chewing, tumor stage, node stage, metastasis, disease stage, lymphovascular invasion, extranodal extension, perineural invasion, and tumor grade were analyzed by chi-square test, and the main endpoints of interest were recurrence-free survival (RFS) and disease-specific survival (DSS) which were analyzed by the Kaplan-Meier method and Cox model.

Fluorescent staining results of typical heterotypic neutrophil-in-tumor structure showed that well-differentiated H157 cells had a stronger ability to internalize more neutrophils than poorly-differentiated H157 cells, with the latter often internalizing only one neutrophil or nothing. The mean FNiT was 4.2‰, with a range from 2.3‰ to 7.8‰. A total of 80 patients relapsed and 84 patients died of the disease. The 5-year RFS and DSS rate was 42% and 42%, respectively. Patients with an FNiT≥4.2‰ had a significantly higher risk for locoregional recurrence and cancer-caused death than those with an FNiT<4.2‰ (p=0.001 and p<0.001, respectively). The FNiT alone was independently significant in predicting poor RFS, and the FNiT along with tumor grade was an independent predictor for DSS.

The FNiT as a novel predictor is significantly negatively associated with both the RFS and DSS of patients with BMSCC.

The FNiT as a novel predictor is significantly negatively associated with both the RFS and DSS of patients with BMSCC.